Almost 500 million individuals suffer from Type I allergy, a genetically determined hypersensitivity disease which is based on the formation of IgE antibodies against per se harmless antigens (i.e., allergens) (1). The symptoms of Type allergy (allergic rhinitis, conjunctivitis and allergic asthma) are mainly caused by the crosslinking of effector-cell bound specific IgE antibodies and the consecutive release of biological mediators (e.g, histamine, leukotriens) (2).
Grasses and corn are distributed worldwide, produce large amounts of pollen which become easily airborn and therefore belong to the most important allergen sources. More than 40% of allergic patients are sensitized against grass pollen allergens of which group 2 allergens represent one of the most frequently recognized allergens (3, 4). Group 2 allergens occur in pollen of many grass species as highly homologous proteins with a molecular weight of approximately 10-11 kDa. Approximately 70% of grass pollen allergic people are cross-sensitized to group 2 allergens which is due to sequence, structural, and immunological similarities of group 2 allergens from different grass and corn species (5-7). Recombinant Phl p 2 from timothy grass has been produced as immunologically active recombinant protein which equals the properties of the natural allergen (6). Moreover the three dimensional structure of rPhl p 2 has been recently determined by NMR analysis and was found to resemble structural features of an immunoglobulin-like domain (8).
Specific therapy of Type I allergy can be achieved in principle by active and passive vaccination. Active vaccination is achieved by specific immunotherapy in order to induce unresponsiveness towards allergens. Although successfully practised since 1911, the immunologically mechanisms of specific immunotherapy are not completely understood (9, 10). Induction of blocking antibodies of the IgG class which interfere with the IgE allergen interaction, modulation of T cell and effector cell responses and generation of tolerance are discussed as possible mechanisms (11). In contrast to active vaccination, passive vaccination is based on the transfer of protective immunoglobulins and represents a routine treatment for many infectious diseases (e.g., hepatitis). The therapeutical efficacy of “passive vaccination” for the treatment of Type I allergy has been demonstrated by classical experiments more than 60 years ago. In 1935 Cooke and collegues reported cure of a hayfever patient by transfer of blood from a patient who had been successfully treated by specific immunotherapy (12). A few years later Loveless showed that the protective effects reported by Cooke are due to blocking antibodies (13) There are several arguments why blocking antibodies may be useful for passive therapy of Type I allergy. First, IgE is the least abundant class of immunoglobulins which could be easily competed. Second, allergic reactions occur in target organs (nose, eyes, lung, skin) where it would be easy to apply blocking antibodies or other competitors of the IgE-allergen interaction avoiding the need of systemic application. The application of the “passive vaccination concept” for treatment of Type I allergy requires however progress in the field of allergen characterization and antibody technology.